摘要
Exaggerated plasma concentrations of GLP-1 precede reactive hypoglycemia after oral glucose in gastrectomy patients, resulting in late dumping syndrome. Rece ntly, we showed that GLP-1 elicits the activation of sympathetic outflow. Because sympathetic activation is thought to be a cause of early dumping, we hypothesized that exaggerated GLP-1 may contribute to the pathophysiology of early dumping syndrome. In 11 patients after gastrectomy and 14 controls, blood pressure, heartrate, and plasma concentrations of norepinephrine, epinephrine, GLP-1, gluca- gon, insulin, and glucose were measured after oral glucose. In gastrectomy pat ients, GLP-1, norepinephrine, and heart rate peaked 15 to 30 min after oral glu cose. Significant positive correlations were found among GLP-1, norepinephrine, and heart rate at 30 min, and these parameters at 30 min were significantly hig her in patients with early dumping syndrome. These results suggest that GLP-1 i s involved in the pathophysiology of early dumping syndrome.
Exaggerated plasma concentrations of GLP-1 precede reactive hypoglycemia after oral glucose in gastrectomy patients, resulting in late dumping syndrome. Rece ntly, we showed that GLP-1 elicits the activation of sympathetic outflow. Because sympathetic activation is thought to be a cause of early dumping, we hypothesized that exaggerated GLP-1 may contribute to the pathophysiology of early dumping syndrome. In 11 patients after gastrectomy and 14 controls, blood pressure, heartrate, and plasma concentrations of norepinephrine, epinephrine, GLP-1, gluca- gon, insulin, and glucose were measured after oral glucose. In gastrectomy pat ients, GLP-1, norepinephrine, and heart rate peaked 15 to 30 min after oral glu cose. Significant positive correlations were found among GLP-1, norepinephrine, and heart rate at 30 min, and these parameters at 30 min were significantly hig her in patients with early dumping syndrome. These results suggest that GLP-1 i s involved in the pathophysiology of early dumping syndrome.
